Various beta adrenergic agonists that increase the accumulation of cAMP are known to induce pineal N-acetyltransferase (NACT) activity. Even though beta adrenergic receptors control both cAMP and cGMP accumulation, cGMP has no apparent role in the increase of NACT. Histochemical localization of cyclic nucleotide indicates that even though most of the cGMP is localized in the nerve innervating the gland it also appears to be present in pinealocytes, even in denervated glands, and catecholamines are markedly decreased. It is possible that cGMP may play a role in the catecholamine and serotonin secretion from the nerve ending in the pineal gland. Studies in isolated pinealocytes from newborn rats indicate that only cAMP is increased 100-200 fold by various catecholamines which is associated with the induction of NACT. cAMP appears to be necessary for maintaining the activity of NACT since lowering of cAMP causes an immediate lowering of the enzyme activity in the pinealocyte and is reversed by dibutyryl cAMP.